This invention relates generally to the field of cardiac pacemakers, and more particularly, to a pacemaker having an escape interval which is set in response to a measured physiologic variable of the patient.
When the body undergoes exercise, a variety of changes take place. These include an increase in respiration, diversion of blood flow to the active skelletal muscles, and an increase in cardiac output. These changes cooperate to deliver an increased amount of oxygen and nutrients to the active muscles.
The mass flow rate of oxygenated blood from the heart is referred to as the cardiac output of the heart, and it is equal to the product of the heart rate in beats per minute and the heart's stroke volume in liters.
The increase in cardiac output is achieved by an increase in the stroke volume of the heart; up to two fold, as well as an increase in the heart rate; up to three fold.
The changes in stroke volume are mediated by venous return, contractility and afterload, while the changes in the heart's rate are mediated through the autonomic nervous system which operates on a structure called the S-A Node.
The S-A Node is located on the atria of the heart. An electrical signal generated by this natural pacemaker causes the atria, or upper chambers of the heart to contract. This forces blood into the lower chambers or ventricles of the heart. The signal from the S-A Node is propagated to the lower chambers of the heart through a structure called the Atrio-Ventricular or A-V Node after a brief delay. The signal from the A-V Node causes the ventricles to contract, forcing the blood throughout the body.
Many forms of heart disease impare the function of the S-A and A-V Nodes, and their associated conductive tissues. Patients exhibiting these indications may be candidates for artificial pacemaker therapy.
Initially, pacemakers were implanted in patients who exhibited complete A-V block. This conduction disturbance is manifested by the inability of the signal from the S-A Node to reach the lower chambers of the heart to initiate a ventricular contraction.
The earliest form of implantable pacemaker for the long-term stimulation of the heart is known from U.S. Pat. No. 3,057,356 issued to W. Greatbatch. This asynchronous pacemaker, in essence, replaced the heart's natural conduction system and periodically provided an electrical stimulus to the ventricle to cause contractions.
In some patients, the A-V block condition is intermittant and occasionally the artificial pacemaker and the natural S-A Node of the heart complete for control of the ventricular action of the heart. This competition is undesirable. The demand pacemaker avoids this competitive pacing. An example of an implantable version of the demand pacemaker is known from U.S. Pat. No. 3,478,746, to W. Greatbatch.
In operation, the demand mode pacemaker senses the ventricular contraction of the heart, and provides stimulation to the ventricles only in the absence of a naturally occurring contractions of the heart. Such demand pacemakers synchronize their timing with the heart and provide stimulated beats if the natural cardiac rhythm drops below a preset rate. Both the asynchronous and demand type of pacemaker thus provided for a fixed lower rate for the patient's heart rate.
When a patient has no intrinsic rhythm and is being paced at a fixed rate, any increment in demand for cardiac output must come solely from naturally induced changes in stroke volume. For these patients, strenous work is impossible since stroke volume changes alone are insufficient to raise the cardiac output enough to supply the skeletal muscles during heavy exercise.
By way of contrast, the P-synchronous mode of pacemaker, as exemplified by U.S. Pat. No. 3,253,596 to J. W. Keller, monitored electrical activity in the atrium, and triggered a ventricular action after a short time period. This form of pacemaker permits the patient's naturally occurring atrial rate to control the rate of ventricular stimulation.
Other pacemakers which exhibit the atrial tracking feature include the atrial-synchronized, ventricularly inhibited pacemaker known from U.S. Pat. No. 3,648,707 to W. Greatbatch, as well as the dual-sense, dual-pace pacemaker known from U.S. Pat. No. 4,312,355 to H. Funke. The advantage of atrial synchronized pacing is that it permits the pacemaker's rate to be determined by the S-A Node which in turn intreprets the body's demand for cardiac output.
Another form of rate adaptive pacer is known from U.S. Pat. No. 4,298,007 to Wright et al. This device monitors the artrial rate and alters the ventricular escape interval in response to the atrial rate.
For these patients, the pacemaker mimics the natural conductive system of the heart and increased demand for cardiac output comes from both an increase in heart rate controlled by the S-A Node as well as concomitant increase in stroke volume.
However, in many patients, the S-A Node is not a reliable source of information concerning the body's demand for cardiac output. Incorporating an S-A Node replacement to provide rate adaptive pacing would be desirable.
One form of rate responsive pacemaker which relies on the detection of blood saturation of oxygen is known from U.S. Pat. No. 4,202,339 to Wirtzfield. This device utilizes an optical measuring probe which is inserted into the heart to monitor the oxygen saturation of the blood. This measurement is then used to alter the stimulating frequency of an associated pacemaker.
Another form of rate responsive pacemaker is known from U.S. Pat. No. 4,009,721 to Alcidi. This device utilizes a pH measurement probe which alters the pacemaker's rate in response to the measurement of blood pH.
Another form of rate adaptive pacemaker is known from U.S. Pat. No. 4,140,132 to Dahl, which utilizes an accelerometer to monitor the physical activity of the patient, and which alters the pacemaker's escape interval.
Another form of rate adaptive pacer is known from U.S. Pat. No. 4,228,803 to Rickards. This patent discloses a pacer which monitors the Q-T interval of the cardiac cycle and increases the pacer rate in response to shortening of the Q-T interval.
Each of the preceding pacemakers has taken advantage of a physiologic parameter which varies with the body's demand for cardiac output.
Returning to cardiac physiology, and in reference to FIG. 3A it is important to note that the cardiac output of the heart, measured in liters of blood per minute, is the product of the patient's heart rate times the stroke volume of the heart. The figure shows a family of constant cardiac output curves called isopleths corresponding to cardaic outputs of 1 to 6 L/M. As previously indicated, increased physical activity in normal individuals, results in an increased cardiac output. In the normal heart, both the heart rate and the stroke volume increase to satisfy the body's need for oxygenated blood. Studies by Versteeg (1981) show that for exercise this cardiac transfer function is a first order linear function with a 10-12 second time constant. This normal cardiac response to increasing work loads is shown by the cardiac load line 300 on FIG. 3a. In the figure, a work load corresponding to cardiac output of 2 L/M is met by a heart rate of 75 bpm at a stroke volume of 26 ml. An increase in work load calling for a cardiac output of 5 L/M is met with a rate increase to 140 bpm and a stroke volume increase to 36 ml.
In those patients who have complete heart block and a fixed-rate pacemaker, it has been noted that increased demand for cardiac output due to physical exertion results in an increase in the measured stroke volume of a patient's heart. This is depicted in FIG. 3b, where the load line 310 corresponds to pacing at a fixed rate, as in asynchronous (VOO), demand pacing (VVI) or A-V sequential (DVI) pacing. This figure indicates that those paced patients who have S-A Node dysfunction can only change stroke volume in response to exercise. For example, at 2 L/M of cardiac output this patient exhibits a stroke volume of 20 ml at a rate of 100 bpm. An increase to 5 L/M calls for a stroke volume increase to 50 ml which may well be beyond the patient's capability.
Thus, the prior art discloses rate adaptive pacers which monitor a physiologic parameter.
Additionally, the response of the heart's stroke volume to physical exertion is well-known in the art.